Abstract
Neonatal Wistar rats were exposed to lead from parturition to weaning via the milk of dams drinking 0.2% lead acetate solution. The alterations in EPSPs in areas CA1 and CA3 of hippocampal slices of 60-day-old adult rats following developmental lead exposure were studied. The results demonstrate that lead exposure in neonatal rats causes a decrease in LTP in area CA1 and an increase in LTP in area CA3. The effects of exposure to NO-generating compound sodium nitroprusside (SNP) on LTP in areas CA1 and CA3 of control and lead-exposed rats were also tested. The data demonstrate that NO causes an increase in LTP in area CA1 and no different alterations in area CA3 of lead-exposed rats. The results also demonstrate that NO may be a messenger molecule in areas CA1 and CA3. It suggests that lead might selectively interfere with specific neurochemical pathways in the hippocampus.
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